``Despair`` gene linked to depression and schizophrenia

Last Updated: Saturday, November 14, 2009 - 00:00

Washington: A gene, touted as the "despair" gene, which earlier had no relation with mood disorders, has now been found to have a link with bipolar disorder, depression, and schizophrenic conditions, according to pharmacy scientists at the University of Maryland, Baltimore (UMB).

The researchers have identified antidepressant and anti-anxiety behaviours in tests of mice lacking the gene.

Dr. Elisabeth Barbier and Dr. Jia Bei Wang ran a series of standard behavioural tests on the mice without the PKCI/HINT1 gene, concluding that it may have an important role in mood regulation.

Mice in the study that had what is being called the "despair" gene eventually gave up trying to avoid apparent danger in tests involving swimming or exposure to light-conditions disliked by mice.

Mice without the gene kept trying to escape from danger, perhaps abnormally.

"The knockout mice [without the gene] displayed behaviours indicative of changes in mood function, such as increased perseverance and reduced anxiety in open spaces," said Wang.

"We don``t yet know why the deletion of the gene altered the mood status of the mice," she added.

She said that the protein encoded by the gene could be a potential target for development of diagnostic or therapeutic agents that one day might be used for depression, bipolar disorders or schizophrenia.

The researchers discovered the gene while studying the biological receptors in brain cells that respond to opioid drugs.

"We are showing the scientific community that this is an important protein that may have something to do with schizophrenia, bipolar [disorders], and depression. But we don``t know how it works. Certainly this opens the door for work on discovering the mechanism, how it changes behaviour. This is the first paper to show that this protein is important to these conditions," she said.

The study has been published in the journal BMC Neuroscience.

ANI



First Published: Saturday, November 14, 2009 - 00:00

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